The hypothesis is postulated that microchimerism arising from pregnancy contributes to the pathogenesis of scleroderma. Five specific aims will be addressed; three test the hypothesis that maternal-fetal-HLA-compatibility increases the risk of subsequent scleroderma. These studies will examine patients and their children as well as patients and their mothers. The remaining two aims will seek proof of non-host cells in the blood and tissues of scleroderma patients. If persistent fetal cells are involved in the pathogenesis of scleroderma, they could be targeted for selective elimination.